Analyzing the effects of DMARD treatment on genetic expression
Anna Boateng (s175562), Marlies Goedknegt (s220675), Anne Gjelstrup (s194530), Katja Jagd (s185395), Olivia Ronnenberg (s183359)
Introduction
Genome-wide transcriptional effects in RA (rheumatoid arthritis) patients, undergoing treatment with several disease-modifying drugs (DMARDs).
What are the genetic differences in RA patients, before and after DMARD treatment?
Materials and Methods
Picture flow chart here
Results: Differential expressed regulators
From the data in table 1 and 2, it can be seen that there is a difference in regulator expression before and after treatment.
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Results: Differential expressed regulators before treatment
First, the plot below shows the genetic expression levels in RA patients, before DMARD treatment.
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Results: Differential expressed regulators after treatment
Secondly, we show genetic expression levels in RA patients, after DMARD treatment.
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Results: Differential expressed regulators after treatment
Lastly, we show a comparison plot to indicate genetic differences as a result of treatment.
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Results: Target molecules
The upstream regulators consisted of several types of biological molecules, serving various functions.
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Results: Target molecules
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Results: Molecular mechanisms
A module is a cluster of related genes, either with related function, common transcriptional regulation, or selectively co-expressed in certain cell types.
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Results: Molecular mechanisms
From this plot, TGFB1 can be a potential drug target.
Discussion
The study by Walsh et.al. found 292 genes down-regulated due to treatment, and 23 up-regulated. The down regulated genes are related to the immune system, a.o. T-cell activating-genes.
This can be explained due to the fact that RA is an auto-immune disease. Less disease activity means less immune activity, and vice versa.
The genetic regulation is based on RA patients, compared to healthy control samples.
Our findings
We identified TGFB1 as a potential drug target.
This finding is based on RA patients before and after DMARD treatment.
TGFB1, and its corresponding “module 2” molecules, are potential drug targets for further investigation.
